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Blood, 15 December 2003, Vol. 102, No. 13, pp. 4555-4562. Prepublished online as a Blood First Edition Paper on August 28, 2003; DOI 10.1182/blood-2003-06-2077. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-06-2077v1 102/13/4555    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Lebigot, I. Articles by Quang, C. T. Search for Related Content PubMed PubMed Citation Articles by Lebigot, I. Articles by Quang, C. T. Related Collections Hematopoiesis and Stem Cells Neoplasia Apoptosis Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Up-regulation of SLAP in FLI-1-transformed erythroblasts interferes with EpoR signaling Ingrid Lebigot, Paola Gardellin, Laurent Lefebvre, Hartmut Beug, Jacques Ghysdael, and Christine Tran Quang From the UMR 146 du Centre National de la Recherche Scientifique (CNRS), Institut Curie, Orsay, France; and Institute of Molecular Pathology, Vienna, Austria. Rearrangement of the FLI-1 locus and ensuing overexpression of FLI-1 protein is an early event in Friend murine leukemia virus (F-MuLV)-induced erythroleukemia. When overexpressed in primary erythroblasts, FLI-1 converts erythropoietin (Epo)-induced terminal differentiation into a proliferative response. We found that SLAP, a gene encoding a recently described negative regulator of T-cell antigen receptor function during thymocyte development, is up-regulated both at the RNA and protein levels in FLI-1-transformed erythroblasts. Src-like adaptor protein (SLAP) was found in a specific complex with erythropoietin receptor (EpoR), a cytokine receptor essential to erythroid differentiation. Constitutive expression of SLAP severely impairs hemoglobinization and late survival during Epo-induced terminal differentiation of erythroblasts. This impairment is associated with the specific inhibition of several critical Epo-dependent signaling events, including signal transducer and activator of transcription 5 (STAT5) activation and up-regulation of the expression of the antiapoptotic BCL-X gene. Our data support a model by which FLI-1 inhibits normal erythroid differentiation through the deregulation of genes encoding adaptors/effectors that modify the signaling output of cytokine receptors normally required for terminal differentiation. (Blood. 2003; 102:4555-4562) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: G. Juban, G. Giraud, B. Guyot, S. Belin, J.-J. Diaz, J. Starck, C. Guillouf, F. Moreau-Gachelin, and F. Morle Spi-1 and Fli-1 Directly Activate Common Target Genes Involved in Ribosome Biogenesis in Friend Erythroleukemic Cells Mol. Cell. Biol., May 15, 2009; 29(10): 2852 - 2864. [Abstract] [Full Text] [PDF] B. Pakuts, C. Debonneville, L. M. Liontos, M. P. Loreto, and C. J. McGlade The Src-like Adaptor Protein 2 Regulates Colony-stimulating Factor-1 Receptor Signaling and Down-regulation J. Biol. Chem., June 22, 2007; 282(25): 17953 - 17963. [Abstract] [Full Text] [PDF] E. van den Akker, S. Ano, H.-M. Shih, L.-C. Wang, M. Pironin, J. J. Palvimo, N. Kotaja, O. Kirsh, A. Dejean, and J. Ghysdael FLI-1 Functionally Interacts with PIASx{alpha}, a Member of the PIAS E3 SUMO Ligase Family J. Biol. Chem., November 11, 2005; 280(45): 38035 - 38046. [Abstract] [Full Text] [PDF]

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